ArticleGastroenterology2024
BRD9-SMAD2/3 Orchestrates Stemness and Tumorigenesis in Pancreatic Ductal Adenocarcinoma.
Article in Gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- BRD proteins in human retroviral infection: emerging evidence from HIV-1 and future perspectives for HTLV-1.Molecular biology reports · 2026Review
- Chromatin Remodeller BRD9 Orchestrates Odontoblastic Differentiation via Coordinating RUNX2-KLF4.Cell proliferation · 2026Article
- Targeting C5AR1 disrupts complement-driven G0-phase maintenance and overcomes metabolic drug resistance in glioma.Journal of translational medicine · 2026Article
- Aberrant activation of epigenetic BRD9-DGAT1 axis promotes lipid droplets deposition and ferroptosis resistance in YAP-high prostate cancer.Cell death & disease · 2026Article
- Review
- Clinical characteristics of programmed death-1 inhibitors for older patients with advanced pancreatic cancer.World journal of gastrointestinal oncology · 2026Article
- Key imidazolyl groups that induce phenylalanine flipping enhance the efficacy of oral BRD9 inhibitors for AML treatment.Acta pharmaceutica Sinica. B · 2025Article
- Targeting SERPINB3-MAPK axis-mediated cuproptosis resistance enhances the response to antitumor immunotherapy.Molecular cancer · 2025Article
- DNA methylation-mediated ADA overexpression drives pancreatic cancer progression.Discover oncology · 2025Article
- Targeting ferroptosis in cancer stem cells: A novel strategy to improve cancer treatment.Genes & diseases · 2025Review
- BRD9-p53-E2F1 circuit orchestrates cell growth and DNA damage repair in gastric cancer.Molecular cancer · 2025Article
- The FOXP1-ABCG2 axis promotes the proliferation of cancer stem cells and induces chemoresistance in pancreatic cancer.Cancer gene therapy · 2025Article
- Multifaceted roles of OCT4 in tumor microenvironment: biology and therapeutic implications.Oncogene · 2025Review
- Chromatin remodeling and cancer: the critical influence of the SWI/SNF complex.Epigenetics & chromatin · 2025Review
- New insights on anti-tumor immunity of CD8Journal of translational medicine · 2025Review
- FOXM1-Driven CKS1B Upregulation Promotes Pancreatic Cancer Progression and Therapeutic Resistance.International journal of biological sciences · 2025Article
- Integrated multi-omics elucidatesFrontiers in immunology · 2025Article
- Current and future immunotherapeutic approaches in pancreatic cancer treatment.Journal of hematology & oncology · 2024Review
- The pRb/RBL2-E2F1/4-GCN5 axis regulates cancer stem cell formation and G0 phase entry/exit by paracrine mechanisms.Nature communications · 2024Article
- BRD9-mediated control of the TGF-β/Activin/Nodal pathway regulates self-renewal and differentiation of human embryonic stem cells and progression of cancer cells.Nucleic acids research · 2023Article
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Authors and funding
25 authors at 8 institutions in 4 countries.
Funding
Abstract
BACKGROUND &
aimsThe dismal prognosis of pancreatic ductal adenocarcinoma (PDAC) is linked to the presence of pancreatic cancer stem-like cells (CSCs) that respond poorly to current chemotherapy regimens. The epigenetic mechanisms regulating CSCs are currently insufficiently understood, which hampers the development of novel strategies for eliminating CSCs.
methodsBy small molecule compound screening targeting 142 epigenetic enzymes, we identified that bromodomain-containing protein BRD9, a component of the BAF histone remodeling complex, is a key chromatin regulator to orchestrate the stemness of pancreatic CSCs via cooperating with the TGFβ/Activin-SMAD2/3 signaling pathway.
resultsInhibition and genetic ablation of BRD9 block the self-renewal, cell cycle entry into G0 phase and invasiveness of CSCs, and improve the sensitivity of CSCs to gemcitabine treatment. In addition, pharmacological inhibition of BRD9 significantly reduced the tumorigenesis in patient-derived xenografts mouse models and eliminated CSCs in tumors from pancreatic cancer patients. Mechanistically, inhibition of BRD9 disrupts enhancer-promoter looping and transcription of stemness genes in CSCs.
conclusionsCollectively, the data suggest BRD9 as a novel therapeutic target for PDAC treatment via modulation of CSC stemness.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.